Suppression of TRPM7 inhibits proliferation, migration, and invasion of malignant human glioma cells

抑制 TRPM7 可抑制恶性人类胶质瘤细胞的增殖、迁移和侵袭

阅读:5
作者:Tian-Dong Leng, Ming-Hua Li, Jian-Feng Shen, Ming-Li Liu, Xin-Bo Li, Hua-Wei Sun, Debbie Branigan, Zhao Zeng, Hong-Fang Si, Jun Li, Jeff Chen, Zhi-Gang Xiong

Aims

We determine the role of TRPM7 channels in the growth, migration, and infiltration of malignant glioma cells.

Background

Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor with a dismal prognosis. Despite intensive study on tumor biology, the underlying mechanisms of the unlimited proliferation and progressive local invasion are still poorly understood, and no effective treatment has been developed for GBM patients. Aims: We determine the role of TRPM7 channels in the growth, migration, and infiltration of malignant glioma cells.

Conclusion

We demonstrate that human glioma cells express functional TRPM7 channel and that activation of this channel plays an important role in the proliferation, migration, and invasion of malignant glioma cells. TRPM7 channel may represent a novel and promising target for therapeutic intervention of malignant glioma.

Methods

Using a combination of RT-PCR, Western blot, and patch-clamp techniques, we demonstrated the expression of functional TRPM7 channels of A172 cells, a human glioma cell line, as well as in human glioma tissues. Furthermore, we evaluated the role of TRPM7 in growth, migration, and infiltration of A172 cells with MTT and transwell migration and invasion assays.

Results

We showed the expression of functional TRPM7 channels in both A172 cells and human glioma tissues. Suppression of TRPM7 expression with TRPM7-siRNA dramatically reduced the proliferation, migration, and invasion of A172 cells. Pharmacological inhibition of TRPM7 channel with 2-aminoethoxydiphenyl borate (2-APB) showed a similar effect as TRPM7-siRNA.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。